The Handiest Girlie Of All

Experimental drug helps the brain recover from stroke -- in mice

In mouse experiments, an experimental drug helped repair damage in the brain induced by a stroke, according to a new study.

 

Scientists have developed a “proof of concept” drug for stroke patients that helped afflicted mice recover the ability to walk normally. In laboratory experiments, the researchers also found biological evidence that the drug helped grow new neurons in the brain, according to a study published online Tuesday by the journal Stroke.

An estimated 795,000 Americans have a stroke each year, according to the National Stroke Assn. in Centennial, Colo.  They occur when the brain is suddenly deprived of oxygen and nutrients, either by a blockage in a vessel (which causes an ischemic stroke) or due to a burst vessel that causes bleeding in the brain (a hemorrhagic stroke). Either way, a stroke can leave patients with weakness or paralysis on one side of the body and “cause problems with thinking, awareness, attention, learning, judgement, and memory,” among other problems, according to the National Institute of Neurological Disorders and Stroke.

Though stroke is a major cause of long-term disability, the only proven treatment for patients is to dissolve a clot or stop the bleeding in the brain while the stroke is happening. Once it’s over, doctors and therapists can only offer rehabilitation to minimize the damage. The experimental drug being developed by scientists from Stanford University School of Medicine, Weill Cornell Medical College and UC San Francisco aims to change that.

The drug is designed to mimic a protein called brain-derived neurotrophic factor, or BDNF, which is thought to help stimulate growth of new neurons and make the brain “plastic,” or able to adapt to changes. BDNF works in cooperation with a receptor in the brain called TrkB. So the scientists set out to find a way to activate TrkB in hopes that doing so would mimic the action of BDNF and promote actual healing in the brain.

The researchers turned to a small molecule called LM22A-4 that – like BDNF – is known to bind to TrkB. The compound was made by a company called Ricerca Biosciences.

To test its stroke-healing powers, the research team used 4-month-old mice and trained them to perform several physical tasks. Then they induced strokes by blocking the right carotid artery in the animals. This caused the mice to perform worse on tasks that they used to do with ease, such as walk across a horizontal ladder and keep their balance on a spinning rod (picture a lumberjack in a log-rolling competition).

Three days after the strokes, some of the mice were treated with LM22A-4, delivered through their noses, while others got a placebo. Mice in both groups recovered well enough to walk across a horizontal ladder, but the animals that got the experimental drug recovered significantly faster, according to the study.

Looking at another mobility measure, the researchers found that the mice in the placebo group saw their “swing speed” decline by 50% and stay there. But mice who got LM22A-4 were able to regain their pre-stroke swing speed.

In the brain itself, the scientists found twice as many new neurons growing in the treated mice compared with their untreated counterparts. Those extra neurons were concentrated around the site of injury, according to the study.

Not only did LM22A-4 help, it did so without causing any harm. The researchers said the drug did not prompt scar tissue to form, boost inflammation or affect the growth of new blood vessels, among other things.

A summary of the study is available online here.

UCSF and the University of North Carolina have already patented the use of LM22A-4 for stroke treatment. One of the Stanford-based study authors has formed a company that is working to turn LM22A-4 and other small molecules into drugs to treat neurological disorders. Of course, any treatment for human stroke victims is still years away.

L.A.TIMES

Taking On Dementia With the Experiences of Normal Life

 

Theo Visser with his wife, Corrie, a dementia patient who cannot speak. She lives in the Hogewey complex in the Netherlands, where residents can walk in the courtyard, go shopping and do other things that are a normal part of life.

 

WEESP, the Netherlands

The sparkling-new 23-unit Hogewey complex here is virtually indistinguishable from other residential developments in the area. The apartments open onto a courtyard with benches, ponds and fountains, with beds of flowers in season (this is the Netherlands, after all). One kidney-shaped pond planted with reeds and other vegetation occasionally attracts wild ducks.

 

There are plenty of amenities: a small supermarket, a theater and a restaurant and cafe that attract people from around the area. Again, nice, but nothing out of the ordinary. The residents can also participate in a variety of activities, like clubs for music, baking, painting and gardening.

Yet, if Hogewey does not sound all that different from a typical residential complex, that is exactly the point. The residents are older men and women suffering from severe dementia, but instead of being constrained in a typical nursing home, they live here for $6,555 a month, six to eight to an apartment, where they are cared for by two or more trained professionals.

The Hogewey complex is in Weesp, a city of 18,000.

 

The residents are confined to Hogewey for their own safety. But within the complex they are allowed to move around freely, to the extent that they are able. On a recent unseasonably chilly afternoon, the residents of one apartment, designated as “urban” to reflect its residents’ tastes, gathered around a dining room table for tea. Most sat quietly, smiling, some in wheelchairs. Jo Verhoef, a woman known as Aunt Jo, sat upright in a comfortable armchair.

“Sometimes we shop, sometimes we listen to classical music,” she said with a smile, summoning her high school English to converse with a visitor. “My father liked classical music. My father was the music man.”

 

Theo Visser’s wife, Corrie, who uses a wheelchair, does not speak, but she enjoys the company. Mr. Visser, 81, said conditions could be difficult, as when a staff member fell sick last year and a substitute took over. “Now, there’s more togetherness,” he said, though he admitted that his wife’s inability to talk made it hard for her.

The idea behind Hogewey developed over the last 20 years. But it was only after the new quarters were built in 2009 that it began attracting attention as a humane and cost-effective response to a disease that is claiming an increasing number of victims as life expectancies in the developed world continue to rise.

In a report released this month, the World Health Organization forecast that the number of people suffering from dementia would double by 2030, to more than 65 million, and triple by 2050, as the world’s population ages. The increase comes as governments everywhere struggle to contain the runaway costs of health care.

“We are receiving attention from our German colleagues, from England,” said Jannette Spiering, the director of Hogewey. “Everyone is struggling with the same problem.” So strong has the attention become that the complex has hired a public information officer to channel the flow of visitors.

Ms. Spiering first began working with dementia patients in a conventional multistory high-rise next door to where the apartments now stand. Over time, she and her colleagues came to feel that their patients would suffer less stress if they were in more familiar surroundings and kept as active as their condition allowed.

So they began rearranging the rooms in the building, creating living spaces and dining areas with mobile kitchens so that the patients, living together in small groups, might experience the smells and sounds of a normal household. “We installed a little supermarket,” said Yvonne van Amerongen, who helped Ms. Spiering in the early days and is now responsible for quality and innovation. “Shopping is part of the daily routine.”

They also created lots of communal spaces. “A demented person,” Ms. Amerongen said, “doesn’t like to sit alone.”

When the home’s operator, a government-owned nursing home group called Vivium, decided to build new facilities, the design reflected those changes. The 240 staff members wear street clothes — there are no white lab coats — but the work is never-ending, as they cook and care for the 152 residents, bathe them and organize their activities. “For the people who work here, it is hard; they are on their own,” said Marjolein de Visser, 23, one of four social workers who make the rounds of the apartments.

She and her colleagues also assist family members. “There’s a lot of guilt, because you’re not taking care of them,” she said.

Dr. Anneke van der Plaats, a geriatrician and adviser to Hogewey, likes the way residents are urged to help with the cooking, with the laundry or with one another. “If you are demented, it is great if you can help other people,” she said over coffee in the complex’s restaurant. “A demented person doesn’t have to sit alone.”

Money has been an issue from the start. When the apartments were built, the cost was estimated at $25.2 million, of which the government put up $22 million. “We had a deficit, and we were creative in closing the gap,” Ms. Spiering said. To generate income, she opened the restaurant and cafe to the public and began renting out the theater for conferences and performances. “We are not a rich nursing home,” she said.

For about a year now, Christian Zierleyn, a former computer consultant, has been responsible for health care in the city government of Weesp, population 18,000. He appreciates Ms. Spiering’s approach to finance, but even more so her opening the complex to the wider public.

Mr. Zierleyn, 42, recently encountered the chief executive of a local bakery goods company, Bakels Senior, which was holding daylong training sessions for customers in the theater, with lunch in the restaurant and a drink in the cafe. At a five-minute walk from the company’s headquarters, it was very convenient.

“He told me his customers were quite suspect at first,” Mr. Zierleyn said. “But in the end they were all very enthusiastic.”

New York Times

Related articles

• The Netherlands: Normal Life for Dementia Patients (themoderatevoice.com)
• Welcome to "Dementia Village," a European Experiment in Long-term Alzheimer's Care (leggotunglei808.wordpress.com)
• A new way of dealing with Dementia (kimhatton.com)

Canadian Hip Hop producer opens up about having MS. "The Beat Goes On"

 

Editor's note:

 In the Human Factor, we profile survivors who have overcome the odds. Confronting a life obstacle – injury, illness or other hardship – they tapped their inner strength and found resilience they didn't know they possessed. This week Chief Medical Correspondent Dr. Sanjay Gupta introduces us to Noah “40” Shebib, a music producer who was diagnosed with multiple sclerosis in his early 20s.

 

 

Q: What was it like to receive that diagnosis as such a young man?

A: It started with sensory issues. I woke up one day and all the temperature in my body was distorted. My sense of hot and cold and what that meant to my brain was very confusing.  Any time something like that happens to your body - which is very difficult to explain when you have MS - is that your brain is tricked, so your nerves are telling you something that's not true.  Any time your brain is telling you something that's not true, there's a little bit of trauma for your body in general to understand what's going on, so you're a little bit in shock.

I went to the hospital very quickly after that and was diagnosed within a couple of weeks. It continued to escalate to a much worse place in a month, and I spent the next two years of my life getting back on my feet.

Q: What exactly were your sensory problems like?

A: It's a funny story. My leg was just on fire when I woke up one day. I was at the studio. I had fallen asleep and had woken up at 2 o’clock in the afternoon the next day, and my first initial thought was, “Oh, I must've fallen asleep by the heater or something.  My leg is really hot.” Then I got in my car and the floor heater was only on, on the left side. I thought, “That's interesting.”

You know, you have all these other explanations except that your brain is telling you something that's not true.  Then I get home and I sit down at my computer, and I'm thinking the heater is just blasting hot air down there. “Where is that heat coming from?”  Then I put on my boots and I said, “Oh my god, this boot is really hot.  This boot must've been beside the heater.”

You always have an explanation, and of course it led me to understand that something was definitely wrong, which led me to the hospital, and as I said – by the end of that month – I was off my feet and not walking.

Q: What was it like to be off your feet, unable to control your own body?

A: I would say it was inspiring, as bizarre and twisted as that may sound.  I tried to see the best light of it and how I could use it to my advantage.

In an almost shallow twisted way, I said, “I’ve got this disease I'm going to live with it.  I'm going to win with it and my story is going to be that much better when I get there.”  I made that decision very early on in my diagnosis.

I remember lying in my hospital bed and they have the little table they swing across your bed to put your meal on, and I quickly put my meal on the chair beside me, put my laptop and the little keyboard, and went directly to work in the hospital bed.  Luckily enough for me, I don't think anything will ever be able to stop me from making music.

Q: What’s the hardest part of dealing with your disease?

A: I think one of the biggest struggles people with MS face is trying to define it to people and explain how it manifests itself.  It's very difficult, you know.  This morning I had to lie down on my bed to get my socks on because I couldn't bend over. You know, that's not something I tell anybody.  Then the things that I deal with on a daily basis are usually pretty miniscule, so I keep them to myself, but they add up, and it's hard for people to understand that.

So I'll say to someone, “Oh, I can't do that today.  They’ll say, “Yeah, but you were playing basketball with us yesterday.”  They don't understand why or how, and it doesn't make sense to a lot of people.  It's very difficult to grasp the concept.

People are confused, so they result to the obvious answer. "Oh well, that's probably because this happened.  Oh, that happens to everybody. Everybody's tired today.  Oh, we've all had a long week."  That's the most frustrating thing for me in the world, because you're taking for granted how hard I work to be on this level with you.

I try to stay quiet about that stuff.  I don't need to have a parade about how hard I'm working.  It's just exhausting explaining to people what you have to deal with if you're trying to keep it quiet and just trying to live a normal life.

Q: People ask why don’t you just try harder, get a little more sleep, or have another cup of coffee?

A: It's funny, you know, one of the things I deal with is sports.  I played hockey my whole life.  When I was diagnosed, I was probably on the ice 5 or 6 times a week at that time.  I haven't really stepped on since.  Every few years, I stop myself and say, "What are you doing?  Why don't you go play some sports?  Stop being such a baby!  Get out there!"

The first time I did that, I was on the ski kill and got stuck halfway down because my legs went numb on me.  I was on the snow for about 40 minutes before my friends came and rescued me and dragged me down the hill.  Then another couple years go by and I think to myself,  "What are you doing? Come on!  Go play some hockey!"  I jump on the ice and skate with some friends and then don't walk for a week after that.

I'm constantly forgetting even myself what the repercussions of my disease are.  I'll be like, "Come on! Get up! You can do this!"  So not only is it difficult for someone else to understand, it's also difficult for me to understand.

CNN/HEALTH

National MS Sociaty

Related articles

• Wired 25: The 25 Most Important People In Hip-Hop Under 25 (hiphopwired.com)
• Producer Mr. Bangladesh says hip-hop has become too safe (thegrio.com)
• Burlington woman grateful for MS Society's assistance (insidehalton.com)

OWN Documentary Club- 65_RedRoses Premieres May 3rd

65_RedRoses - Trailer
65_RedRoses is a documentary that takes an unflinching look into the life of Eva Markvoort as she battles a fatal genetic disease called Cystic Fibrosis. At 23, Eva needs a double lung transplant to live. The film follows her journey to transplant while seeking support from her two online friends Kina and Meg who also have CF.
 

About the Campaign

When Eva Markvoort agreed to open up her life through the documentary 65_RedRoses, the result was a powerful message of life, love, and hope. By doing so, she started a global campaign for organ donation and CF awareness.

While waiting for a second transplant on March 27, 2010, at the age of 25, Eva’s breath ran out. But her vision did not die. Canadian distributor Hello Cool World is working with the filmmakers and Eva’s family to spearhead a North American campaign, centred around the 65RedRoses.com site. The #4Eva Campaign for Organ Donation and CF Awareness is gaining momentum as non-profit partners and supporters get on board. Upcoming campaign activities include a limited theatrical release in Canada, a Special Edition DVD release and an educational package and teachers guide for high schools. Watch for our PSAs across Canada.

To date, the award-winning film has screened at numerous international festivals and been televised in a dozen countries.

It has been chosen for OWN Documentary Club in the US with a US broadcast premiere on May 3rd 9/8c in tandem with the Hello Cool World launch of the 65_RedRoses free #4Eva mobile app. The app will be available free in Canada and the US on all devices, and will encourage people to become organ donors and to spread the campaign to their contacts via social networks.

 

What Is Cystic Fibrosis?

Cystic fibrosis is an inherited chronic disease that affects the lungs and digestive system of about 30,000 children and adults in the United States (70,000 worldwide). A defective gene and its protein product cause the body to produce unusually thick, sticky mucus that:

• clogs the lungs and leads to life-threatening lung infections; and
• obstructs the pancreas and stops natural enzymes from helping the body break down and absorb food.

In the 1950s, few children with cystic fibrosis lived to attend elementary school. Today, advances in research and medical treatments have further enhanced and extended life for children and adults with CF. Many people with the disease can now expect to live into their 30s, 40s and beyond.

 

65_REDROSESS

OWN Documentary Club

Cystic Fibrosis Canada

Cystic Fibrosis Foundation (US) 

Related articles

• breathlessness - thinking of eva markvoort. (lucialorenzi.wordpress.com)
• Ottawa woman stirring after double lung transplant (ctv.ca)
• Big Advance Against Cystic Fibrosis (InnovationToronto.com)
• Day 117 - 65 Roses or Cystic Fibrosis? (ianspagnolo.com)

Life, Interrupted: Facing Cancer in Your 20s

 

 

 

Today, I’m writing from a hospital bed in New York City. I’m in the bone marrow transplant unit, where this week I’ve undergone 20 intensive chemotherapy treatments in anticipation of receiving my brother’s stem cells. In the year since my diagnosis with leukemia, I’ve struggled to hold onto a sense of who I am while I watch the person in the mirror change.

Looking back, I call the first month after my diagnosis “the cancer bubble” because I wasn’t showing obvious signs of my disease. I looked about the same — maybe a little more tired and pale than usual, but a stranger could never have guessed that I carried a secret, deep in my bones.

In the oncology ward, I still felt invisible, flying under the radar with my waist-length hair and the nose ring I got when I was 14. In the waiting room at my second appointment, a man with a sleeveless shirt and a bandanna covering his hairless head leaned in toward my father, who’s been bald since the ’80s, and raised his fist in the air: “Live strong, brother,” he said. Later, my dad and I had a good laugh about the mix-up — it helped ease our tight nerves for a moment. But I remember also feeling slighted, as though my terrible new disease wasn’t being acknowledged.

 

Suleika Jaouad is undergoing a bone marrow transplant for leukemia.

I remember my first day of chemo as if it were yesterday, hanging up my favorite summer dress like an athlete retiring a jersey. Within a few weeks, my waist had shrunk to a double zero — the size it was when I was in the sixth grade. My cheek bones jutting out. Rings under my eyes. Skin the color of chalk. And then there was my hair. My long, wavy hair — the same unruly locks I’d spent countless hours fussing over in front of a bathroom mirror — soon to be gone.

When I finally returned home after my five-week hospitalization, I could feel the stares of strangers on my bald head and thinning eyebrows. Everywhere I went, cancer spoke for me before I could say the first word. Once, I even overheard a child asking her mother why there was a boy in the girls’ bathroom.

Cancer had given me a reverse celebrity status: all the attention for something you didn’t want to be known for. I had crossed over into a new land, the land of Patient. And with every step I was feeling less like Suleika.

Now, here in the bone marrow unit, where I’m required to be in isolation to prevent infections, I’m surrounded 24/7 by the gaze of people who, first and foremost, are concerned with what I have — not necessarily who I am. Doctors in face masks stand over my hospital bed, peering down at me. Eyes and ties. And white lab coats. Voices without mouths discuss me as if I weren’t in the room. They give the Patient a hospital gown. The Patient is talked at, looked at, probed, prodded and whispered about. But after all, it’s their job to see me as Patient. The goal is to cure the Patient so she can return to being herself. But until then, it’s hard not to feel like just a body.

As Patient, you cede control of a lot of your life to others — to your nurses and doctors, to their decisions and schedules. I’m thankful for their care — where would I be without it? But anyone who’s been in the role of Patient can attest to the way it changes how you see yourself.

As I wait for my cure, I’m still a Patient. And while it’s been only a year, I can hardly remember what not being one is like.

NEWYORKTIMES /HEALTH

Secrets of Cancerhood (Suleika Jaouad blog)

Related articles

• Keio docs took marrow without OK (japantimes.co.jp)
• Chemotherapy proves life-saving for some leukemia patients who fail induction therapy (eurekalert.org)
• Bone Marrow Cancer & Primary Bone Cancer Symptoms & Types (cancercenter.com)

iBrain, a Device That Can Read your thoughts

SAN DIEGO,CA

Already surrounded by machines that allow him, painstakingly, to communicate, the physicist Stephen Hawking last summer donned what looked like a rakish black headband that held a feather-light device the size of a small matchbox.Called the iBrain, this simple-looking contraption is part of an experiment that aims to allow Dr. Hawking — long paralyzed by amyotrophic lateral sclerosis, or Lou Gehrig’s disease — to communicate by merely thinking.

The iBrain is part of a new generation of portable neural devices and algorithms intended to monitor and diagnose conditions like sleep apnea, depression and autism. Invented by a team led by Philip Low, a 32-year-old neuroscientist who is chief executive of NeuroVigil, a company based in San Diego, the iBrain is gaining attention as a possible alternative to expensive sleep labs that use rubber and plastic caps riddled with dozens of electrodes and usually require a patient to stay overnight.

“The iBrain can collect data in real time in a person’s own bed, or when they’re watching TV, or doing just about anything,” Dr. Low said.

The device uses a single channel to pick up waves of electrical brain signals, which change with different activities and thoughts, or with the pathologies that accompany brain disorders.

But the raw waves are hard to read because they must pass through the many folds of the brain and then the skull, so they are interpreted with an algorithm that Dr. Low first created for his Ph.D., earned in 2007 at the University of California, San Diego. (The original research, published in The Proceedings of the National Academy of Sciences, was done on zebra finches.)

About the Hawking experiment, he said, “The idea is to see if Stephen can use his mind to create a consistent and repeatable pattern that a computer can translate into, say, a word or letter or a command for a computer.”

The researchers traveled to Dr. Hawking’s offices in Cambridge, England, fitted him with the iBrain headband and asked him “to imagine that he was scrunching his right hand into a ball,” Dr. Low said. “Of course, he can’t actually move his hand, but the motor cortex in his brain can still issue the command and generate electrical waves in his brain.”

The algorithm, called Spears, was able to discern Dr. Hawking’s thoughts as signals, which were represented as a series of spikes on a grid.

“We wanted to see if there was any change in the signal,” Dr. Low said. “And in fact, we did see a change in the signal.” NeuroVigil plans to repeat the study in large populations of patients with A.L.S. and other neurodegenerative diseases.

These preliminary results come as Dr. Hawking’s ability to communicate diminishes as his disease progresses. The 70-year-old physicist, whose mind has produced crucial insights in theoretical physics as well as the best-seller “A Brief History of Time,” now needs several minutes to generate a simple message. He uses a pair of infrared glasses that picks up twitches in his cheek. His team in Cambridge, England, has dubbed this the “cheek switch.”

“Dr. Low and his company have done some outstanding work in this field,” Dr. Hawking said in a statement. “I am participating in this project in the hope that I can offer insights and practical advice to NeuroVigil. I wish to assist in research, encourage investment in this area, and, most importantly, to offer some future hope to people diagnosed with A.L.S. and other neurodegenerative conditions.”

The physicist has also worked with other inventors seeking to better elucidate his thoughts. Engineers at the semiconductor and computing giant Intel recently hooked up a customized computer to communicate with his cheek-reading infrared glasses, along with a voice synthesizer, a webcam for using Skype, and special monitors. Intel is developing new face-recognition software that can monitor subtle changes in expression and may help Dr. Hawking communicate more efficiently.

Scientists not connected with Dr. Low say they are encouraged by the iBrain’s potential. “Philip Low’s device is one of the best single-channel brain monitors out there,” said Ruth O’Hara, an associate professor of psychiatry and behavioral sciences at Stanford University Medical School. She plans to use the iBrain for autism studies. NeuroVigil has not said what the device will cost.

“I can’t speak to the veracity of his latest data,” which has not been published, Dr. O’Hara added, “but the preliminary data I have seen is compelling. It could be a significant contribution to the field as a window into brain architecture.”

Dr. Terry Heiman-Patterson, a neurologist and A.L.S. specialist at the Drexel University College of Medicine, said she was in discussions with NeuroVigil to use the device on A.L.S. patients, to see how they fared with it in comparison with instruments that use multiple channels and electrodes.

“Dr. Low is researching signals that look for intent, which is becoming very exciting because it looks like they may be able to do it — for Stephen Hawking and for others with A.L.S.,” Dr. Heiman-Patterson said.

“Patients want to be able to communicate beyond the yes or no with an eye blink. They want to send an e-mail, and turn off the light and, even more, to have a meaningful conversation.”

Monitors like the iBrain are also being used to assess whether experimental neurological drugs are working in clinical trials.

In 2009, NeuroVigil completed a deal with the drug giant Hoffmann-La Roche to test the iBrain. Neither company has released details of their early tests. NeuroVigil’s strategy, Dr. Low said, is to run clinical trials with Roche and other partners in industry and academia, and to seek approval from the Food and Drug Administration.

Other companies also make single-channel brain monitors, but unlike NeuroVigil they sell the devices and software directly to consumers online.

Zeo, for example, based in Massachusetts, concentrates on measuring sleep patterns through a smartphone app or a clock-radio device — available for $99 and $143, respectively. Emotiv Systems, in San Francisco, offers its Epoc headset for $299 plus a range of apps and add-ons that include neurofeedback, 3-D brain-mapping tools and games like Angry Birds, all using a combination of thoughts and facial muscle movements recorded by several electrodes that are in contact with a customer’s head.

“We have no plans to take an academic route,” said Zeo’s chief executive, Dave Dickinson, who added that his company’s customers had logged one million hours of sleep time. He would not say how many devices had been sold. Emotiv was founded in 2003 and has reportedly shipped 10,000 devices.

Dr. Low plans to team up again with Dr. Hawking this summer in Cambridge to present their initial data at a neuroscience meeting in early July. NeuroVigil will continue to work with Dr. Hawking and his team to refine their technology to decipher signals generated by Dr. Hawking’s thoughts. “At the moment I think my cheek switch is faster” than the brain-computer interface, Dr. Hawking said in an e-mail sent by an assistant, “ but should the position change I will try Philip Low’s system.”

Much work remains, however, including the integration of Dr. Hawking’s brain waves with the computers and devices that allow him to communicate.

“Wouldn’t it be wonderful,” Dr. Low said, “to have a mind like Stephen Hawking’s be able to communicate even a little bit better?”

NeuroVigil,Inc

NY Times

 

Related articles

• A Little Device That's Trying to Read Your Thoughts (3quarksdaily.com)
• iBrain to translate Thoughts into Words. (ramanan50.wordpress.com)
• How Genes Organize the Surface of the Brain (neurosciencenews.com)

Stem cell population may hold colon cancer clues

 Vanderbilt-Ingram Cancer Center researchers have identified a new population of intestinal stem cells that may hold clues to the origin of colorectal cancer.

This new stem cell population, reported March 30 in the journal Cell, appears to be relatively quiescent (inactive) – in contrast to the recent discovery of intestinal stem cells that multiply rapidly — and is marked by a protein, Lrig1, that may act as a “brake” on cell growth and proliferation.

The researchers have also developed a new and clinically relevant mouse model of colorectal cancer that investigators can now use to better understand where and how the disease arises, as well as for probing new therapeutic targets.

Colorectal cancer is the second leading cause of cancer deaths in the United States. These tumors are thought to arise from a series of mutations in intestinal stem cells, which are long-lived, self-renewing cells that gives rise to all cell types in the intestinal tract.

For more than 30 years, scientists believed that intestinal stem cells were primarily quiescent, proliferating only rarely in order to protect the tissue against cancer. Then, in 2007, researchers reported finding a population of intestinal stem cells (marked by the molecule Lgr5) that were highly proliferative.

Those findings “really changed the way we think about intestinal stem cells,” said Robert Coffey Jr., M.D., Ingram Professor of Cancer Research, co-chair of Vanderbilt’s Epithelial Biology Center and senior author on the study.

“It came to so dominate the field that it raised the question about whether quiescent stem cells even exist…and that’s where we enter into the picture.”

Coffey’s lab studies the epidermal growth factor (EGF) signaling pathway — which includes a family of receptors known as ErbBs — and its role in cancers of epithelial tissues, like the intestinal tract.

Postdoctoral fellow Anne Powell, Ph.D., led the recent experiments showing that Lrig1, a molecule that regulates ErbB activity, is present in intestinal cells that have the qualities of stem cells (self-renewal, and the ability to produce all the cells of the intestine).

“Essentially, what we show is that the Lrig1-expressing cells are stem cells and they are largely quiescent,” Powell said. “We also show that they’re distinct from the Lgr5-expressing stem cells that had become a sort of ‘hallmark’ stem cell population…with different gene expression profiles and different proliferative status.”

They also showed that Lrig1 is not only a marker of intestinal stem cells, but also acts as a tumor suppressor and inhibits the growth and proliferative signals of the ErbB family — acting as a sort of “brake” on cell proliferation that can lead to cancer.

Postdoctoral fellow Yang Wang, Ph.D., eliminated Lrig1 in mice and showed that nearly all of those mice developed intestinal tumors, providing further evidence suggesting that Lrig1 functions as a tumor suppressor.

The findings underscore the importance of ErbB signaling in the behavior of intestinal stem cells from which colorectal cancer may arise.

Most exciting, said Coffey, is that the mouse model his lab has generated as a part of these studies is one of the only mouse models to develop tumors in the section of the intestines where most human tumors develop: the colon.

One additional advantage of this model, in contrast to others, is that the tumors develop quickly and can be easily monitored with endoscopy, which will make it easier to assess how therapeutic interventions are working.

“We are fairly confident that this will be the ‘go-to’ model to study colon cancer in mice for the foreseeable future,” Coffey said.

Emily Poulin, Jim Higginbotham, Ph.D., and Jeff Franklin, Ph.D., (from the Coffey lab), Kay Washington, M.D., Ph.D., and Yu Shyr, Ph.D., contributed to the research.

The work was funded by grants from the National Cancer Institute and the National Institute of General Medical Sciences of the National Institutes of Health.

 

Vanderbilt

Related articles

• [读书笔记]Cancer stem cell and heterogeneity (zhihuazhang.wordpress.com)

Frontotemporal Disease-Little-known brain disease rips apart lives of victim, loved ones

Watch NYT video of Loosing Stu

Click here

 

 

More than a year after the diagnosis, Maureen Bryant had grown accustomed to making excuses for her husband.

When Stu stood behind a tattooed woman in line at Panda Express, and said loudly, "Wow, that's a lot of tattoos," Moe stepped between him and the woman and apologized.

When he repeatedly wandered into the house that was being built down the street — despite the "No Trespassing" sign and the fence — she explained to the owner that he was just curious.

Possibly the most embarrassing episode occurred when they were coming home from dinner, and she dashed into a mini-mart at a marina in Oxnard to buy milk.

"Do you know that man?" the owner said, seeing Stu in the car. "He's been stealing from me."

Moe remembers being baffled.

Muffins and cheesecake, the owner said, showing her photos from the store's video camera. "But I can't catch him. He drives away in the golf cart too fast."

Moe offered to pay for what Stu had taken. "He has no control over what he does," she said to police when they arrived.

Sometimes she will say that he has a brain tumor. It's easier than saying frontotemporal dementia and having to describe how the disease has stripped away his self-restraint. Stu is no longer aware of how to behave in the company of others, and like an unknowing child, will blurt out the first thing that comes to mind or will act without considering the consequences.

Moe realizes that this is difficult to understand. Being rude or disrespectful seems like a deliberate choice, and Stu, 60, has a quick smile and an easy laugh. It's easy for people to write him off as inconsiderate and self-centered.

This is what Moe and her daughters, Katy and Jessica, did before they discovered how sick he was.
 

Once called Pick's disease and now FTD, frontotemporal dementia hides its symptoms well. Like Alzheimer's, it is the result of the degeneration of neurons caused by an abnormal accumulation of proteins in the brain.

In early stages, Alzheimer's affects predominantly the hippocampus in the inner part of the brain, where memories are formed, and FTD affects the frontal and temporal lobes, above and behind the eyes, where social emotions are formed. Alzheimer's patients sense a fuzziness in their thinking — a word misplaced, a confusion between the past and present — and realize their errors. Most patients with FTD have no such insight into their disease.

Jessica, 22, first noticed her father becoming more selfish and temperamental when they lived in Sacramento. He doted upon his daughters and would do anything for them, but then that seemed to stop. Where once he let Jessica choose what to watch on TV, now he held on to the remote and got angry if she changed the channel.

The tragedy of FTD, according to Mario Mendez, the UCLA neurologist treating Stu, is its elusive diagnosis. The presence of the disease can be confirmed only through an autopsy, and Mendez reached his conclusion about Stu based on specific behaviors and brain scans.

The disease begins with a change in personality that's often seen as volitional. Introverts become extroverts. Once-agreeable employees act rude. Formerly faithful spouses have affairs, and while they acknowledge their transgressions, they are unable to appreciate the implications.me end up institutionalized because their behavior looks like mental illness. Some are incarcerated when they break the law. A diagnosis of FTD led to reduced charges against a New York City physician who cut his initials into the stomach of a patient, and what could have been as many as 25 years in prison ended up as five years' probation.

Researchers believe that between 30,000 and 50,000 people in the United States have FTD. There is no cure, and the disease leads to death, often within eight years, either from accidents or secondary infections.

When Stu began acting differently in 2007, bickering with Jessica, Moe didn't think anything of it. She and Stu had been married more than 25 years. She figured relationships change.
  
He was the dreamer, she the pragmatic one. She was a consultant for a healthcare company, and he was a private golf coach and a car salesman. But his real passion was coaching baseball. According to Jerry Weinstein — who was head coach in the early 1980s at Sacramento City College, where Stu worked — Stu was known for his caustic wit and demanding practices. The players trusted him, Weinstein said.

Moe and Stu had moved to Sacramento from Los Angeles in 1992. His father had just died, and he thought he should be near his mother. But a decade later, when she was in her 80s, he suddenly stopped wanting to see her.

When Moe asked why, he couldn't say, and after his mother died, he became more withdrawn and stubborn. They saw a counselor and decided that leaving Sacramento might help them get over their problems.

Moe found a rental in Oxnard on the strand between the harbor and the ocean. With so many golf courses in the area, she thought, Stu would be able to find a job and play as much as he liked. He worked for a few months and then stopped. They fought, and one day, almost a year after moving to the beach, she came home to find him packing a U-Haul.

He said he was moving back to Sacramento and had no explanation other than "because this is what I'm doing." Moe, 52, still remembers how empty his expression was that May afternoon in 2010. Family members thought he was having an affair.

He rented a one-bedroom apartment. A family friend, Ed Modeste, visited him and found the place nearly empty: a TV, a chair, not much more. Stu rarely contacted the family.

Divorce seemed inevitable. Then one night Katy, 26, called Moe in tears.

She was living in the Monterey area and had invited her father for the weekend. She and Stu went on a bike ride in the hills above Ft. Ord, and he disappeared, showing up two hours later, hardly concerned that they had become separated. The next day at the U.S. Open at Pebble Beach — her Father's Day treat for him — he couldn't stand still or be quiet, and she thought they'd be kicked out.

She insisted that her mother take him to the family doctor; she had never seen her father act this way. Moe flew to Sacramento, and after Stu underwent an MRI, she felt her life shifting again.

Stu, the doctor told her, is in no position to live by himself. You can either proceed with the separation or you can set your feelings aside and treat this like a medical disease.

Moe wasn't ready to forgive Stu any more than she was prepared to be his caretaker or his widow. But she couldn't leave him on his own.

Stu didn't know that he had hurt his family; he had lost his capacity to care. Moe had to explain to friends and family why she took him back after his three-month absence. Most had never heard of FTD; some thought it a weak excuse for a mid-life crisis.

Under the sway of the disease, impulses in Stu's brain went unchecked. He logged 30 miles on his bike in the course of three daily rides and he became agitated if he did not get to the golf course each day. He was in constant motion, snapping his fingers and tapping his toes. He snacked compulsively, especially when Moe wasn't around to stop him.

Reading about the disease, Moe came across the name of Mario Mendez, a professor of neurology and psychiatry at UCLA and the director of the neurobehavior unit at the West Los Angeles Veterans Affairs hospital.

Mendez and Jill Shapira, a nurse practitioner, see FTD patients on Wednesdays, and Moe made their first appointment for Sept. 8, 2010. Mendez and Shapira reassured Moe that with medications and guidance, Stu's more uninhibited, repetitive behaviors could be suppressed.

Moe and Stu also agreed to take part in a study of the disease. Because FTD makes empathy, embarrassment, guilt and shame all the more conspicuous for their absence, Mendez is investigating how social emotions arise out of the physiology of the brain.

Mendez and Shapira ran a number of tests on Stu designed to isolate different parts of the frontal and temporal lobes. Some were written; some were conducted in conversation, and in one instance, Stu looked at photographs of flowers, mountains, road kill and starving children as monitors captured his skin temperature and heart rate.

"What does it mean that people who live in glass houses shouldn't throw stones?" Mendez asked Stu during a follow-up appointment.

"You'd break the glass," Stu said.

Just as he is incapable of interpreting this saying or engaging in abstract thinking, he is similarly unable to decipher social situations and know why insulting a stranger with tattoos, trespassing on private property or stealing is wrong.

In November, Moe and Stu arrived at UCLA for another MRI. Moe hoped to see how far the disease had progressed. Stu lay down inside the huge machine. When the technician asked if he wanted to listen to music, he asked for the Rolling Stones, one of his favorite bands.
"Let It Bleed" began to play.  

The Bryants' living room fronts the dunes. The Channel Islands float on the horizon, and above the garage hangs a sign that reads "Lazy Days."

Moe gives Stu daily tasks — walking the dogs, cleaning windows, feeding the tortoise, vacuuming — to keep him occupied so he won't wander in and out of the house or search for food that she's hidden. She feigns forgetfulness when they talk, so he will exercise his memory. She plans special outings, like a whale-watching trip a few weeks ago.

The recent MRI, according to Mendez, showed only minute changes in Stu's brain over the last year, but Moe is hardly reassured.

Stu recently took Katy's keys and disappeared in her car without telling anyone. On one of his bike rides, he was hit by a car, and though he had a gash on his leg, he worried only about his ruined bike. At dinner the other night, he started to choke, a sign that he's losing control of his chewing and swallowing.

In time, Moe expects him to become more sedentary and apathetic, and she worries how this will change their lives. For now, though, she stays vigilant, letting down her guard only at night when she lies in bed listening to the distant, rolling surf and to Stu breathing in his sleep beside her.

Related articles

• Same Genes Key to Early & Late-Onset Alzheimer's (nlm.nih.gov)
• Genes Linked To Alzheimer's Are The Same For Early- And Late-Onset (medicalnewstoday.com)
• Cracks in the Plaques: Mysteries of Alzheimer's Slowly Yielding to New Research (bellspalsycranialnerves.wordpress.com)

New Drugs Raise Hope for Patients With M.S.

Three years ago, Kristie Salerno Kent, a singer-songwriter, was standing in a security line at the airport on her way home from a gig when her legs went numb. “From the waist down, it felt as though I was trying to walk through a bowl of oatmeal,” said the 38-year-old musician, who has multiple sclerosis.

She inched her way to a security officer, who called for a wheelchair and helped remove her shoes and belt to get her through security. Frightened and embarrassed, she was taken to her gate in a wheelchair.

Three months later, she experienced another flare-up. While giving a live television interview about a short film she had made on living with M.S., she suddenly lost her ability to speak. “It was as if my mouth was packed with marbles,” she said. “I kept trying to say, ‘I’m sorry,’ to the reporter, but nothing came out that made sense.”

The medication she was taking to prevent these attacks was losing its effect, so her doctor suggested she switch to Tysabri, one of the newer, more potent “disease-modifying drugs,” which reduce the severity and frequency of relapses. She also began taking Ampyra, which early last year became the first drug approved to treat any M.S. symptom. She hasn’t had a flare-up since.

After decades of basic research on M.S., the last five years have brought a rapid rollout of new and sophisticated drugs that are changing how this disease is managed and offering patients new hope.

“We have a disease that’s gone from having no treatments 20 years ago to having multiple treatment options,” said Dr. Timothy Coetzee, the chief research officer at the National Multiple Sclerosis Society. “There is a growing recognition that M.S. is becoming a manageable disease.”

In M.S., the body’s immune system damages neurons in the brain and spinal cord, attacking the myelin sheath that insulates these nerves. About 85 percent of patients start out with what is called relapsing-remitting M.S., characterized by flare-ups or attacks that cause lesions to form on the brain and that affect the ability to walk, to see and to control the bladder, among other neurological impairments.

These attacks are short-lived, and patients typically recover from them. But more than half of patients eventually develop a progressive form of M.S., causing the permanent loss of these functions.

Once that happens, many of the treatments are ineffective. But the new drugs may slow, perhaps even prevent, the progression that was once considered inevitable for many patients.

“The drugs we now have are shifting what the natural history of the disease looks like,” said Dr. Coetzee.

Doctors can now choose from eight disease-modifying drugs, which reduce relapses and thereby slow the progression of the disease. Some of the drugs also prevent brain neurons from dying off, now thought to be a major cause of permanent disability.

There have also been advances in treating specific symptoms of M.S. Within the past two years, three medications have been approved specifically for M.S. symptoms: Ampyra to improve walking, Nuedexta for uncontrollable laughing or crying, and Botox for urinary incontinence and spasticity in upper limbs.

“We’re shooting for disease-free status, where someone with M.S. is on a medicine and has no sign of M.S.,” said Dr. Richard Rudick, director of the Mellen Center for Multiple Sclerosis Treatment and Research at the Cleveland Clinic.

The first generation of M.S. drugs included mostly immune-suppressing interferons delivered via injection or infusion. These are still the most widely used, reducing relapses by about one-third. The new drugs are more sophisticated, targeting specific molecules involved in the disease, rather than simply tamping down the immune system to reduce inflammation in the brain.

Just last year, the first oral drug for M.S., Gilenya, gained approval with data showing it cut the relapse rate by 55 percent. Gilenya causes inflammatory cells called lymphocytes to get trapped in lymph nodes so they don’t travel to the brain, where they would damage neurons.

Patients need to be monitored for several potentially serious side effects, including a slowed heart rate and liver and vision problems. One patient recently died 24 hours after starting on Gilenya; the Food and Drug Administration is investigating the cause of the death.

The most potent drug, Tysabri, reduces the relapse rate by about 70 percent, but it comes with a small risk of a fatal brain infection caused by a common virus. Patients may be screened for antibodies to the virus; the risk of infection is considered quite low in those with no sign of the antibodies, and they are given the drug.

At least four other drugs with different mechanisms are in Phase 3 clinical trials and could win approval within the next year, experts say. Some work by protecting nerves from damage.

“There’s a lot of focus on developing drugs that inhibit or stop this neurodegeneration, which we believe is the underlying cause for difficulty walking, leading people to require a wheelchair,” said Dr. Rudick.

One of the new neuroprotective drugs, called BG-12, captured wide attention at an annual international conference on M.S. in Amsterdam in October. Researchers reported a 53 percent reduction in relapses in patients taking it and a greater than 30 percent reduction of permanent disability progression over a two-year period. It also appears to have fewer risks than equally potent drugs like Gilenya.

“This might be the drug that would completely displace the interferons,” said Dr. Timothy L. Vollmer, director of neurology clinical research at the University of Colorado.

Although many doctors start patients on interferons first because of lower risks, there is a growing recognition that treating patients aggressively and early with the newer medications can preserve brain neurons and possibly prevent the progression of the disease.

But treating M.S. is still difficult. Many treatments come with serious side effects and other risks, and some people simply don’t respond to them. Patients progress at different rates, and the symptoms vary from one patient to another. Some people cannot tolerate certain medications.

“The biggest frustration is the huge uncertainty,” said Dr. Jerome J. Graber, an assistant professor of neurology at Montefiore Medical Center in the Bronx. “I still can’t predict who will progress and what’s the best way to treat someone.”

Still, some patients are beginning to see a more hopeful prognosis. After Ms. Salerno Kent started taking Tysabri and Ampyra, her walking improved enough for her to go hiking with husband and son, her speech issues resolved, and she felt much more confident when singing on stage.

“We have so many more options now, and I realize that we no longer have to give up the quality of life because we have M.S.,” she said. “We’ve always expected to deteriorate with time, but I realize that this is not acceptable anymore.”

 

NY Times

 

Related articles

• New Hope for Muliple Sclerosis Patients (well.blogs.nytimes.com)
• Multiple sclerosis (grigoriatsiakmaki.wordpress.com)
• Experimental multiple sclerosis drug shows promise (newsok.com)

Arthritis and Diseases that Affect the Hand and Wrist

Many forms of arthritis and related conditions that affect the joints, muscles and/or bones can cause problems like pain, stiffness and swelling in the wrist and fingers. Other conditions can cause additional problems, such as numbness and tingling, pitted nails, painful ulcers or thickened skin that makes bending the fingers difficult. Here are some possible disease-related problems that affect the hands and wrists.

 

 

Osteoarthritis (OA)

The most common form of arthritis, osteoarthritis is a chronic condition characterized by the breakdown of the cartilage that cushions the ends of the bones where they meet to form joints. This breakdown causes the bones to rub against each other, causing stiffness, pain and loss of movement in the joint. In the hand, the joints most commonly affected by osteoarthritis are the wrist, the joint at the base of the thumb (the basal joint), the joint in the middle of the finger (proximal interphalangeal joint or PIP) and the joint closest to the nail (distal interphalangeal joint or DIP). In the finger joints, OA can lead to the formation of bony knots. In the PIP joint these are call Bouchard's nodes. In the DIP joint they are called Heberden's nodes.

Learn more about osteoarthritis from Arthritis Today
Experts answer your questions about osteoarthritis

 

Rheumatoid arthritis (RA)

 Rheumatoid arthritis is a chronic inflammatory disease of the joints that occurs when the body’s immune system – which normally protects us from infection – mistakenly attacks the synovium, the thin membrane that lines the joints. The result can be joint damage, pain, swelling, inflammation, loss of function and disability. Rheumatoid arthritis commonly affects the wrist and finger joints and can cause deformities that make it difficult to use the hands.
Learn more about rheumatoid arthritis from Arthritis Today.
 

 

Juvenile arthritis (JA)

Juvenile arthritis is the term used todescribe arthritis when it begins before age 16. There are several different types of juvenile arthritis that can cause pain and swelling in the wrist and joints of the hands.

Learn more about juvenile arthritis from Arthritis Today.
 

 

Gout

Gout is a form of  arthritis that occurs when excess uric acid, a bodily waste product circulating in the bloodstream, is deposited as needle-shaped monosodium urate crystals in tissues of the body, including the joints. For many people, the first symptom of gout is excruciating pain and swelling in the big toe – often following a trauma, such as an illness or injury. Subsequent attacks may occur off and on in other joints, including the wrist and joints of the fingers. After years with the disease, lumps of uric acid, called tophi, may form beneath the skin of the hands.

Learn more about gout from Arthritis Today.

 

Reactive arthritis

 Reactive arthritis is a chronic form of arthritis that often occurs following an infection of the genital, urinary or gastrointestinal system. Features of reactive arthritis include inflammation and swelling of the joints, eyes and structures within the gastrointestinal or genitourinary tracts, such as intestines, kidneys or bladder. A small percentage of people with the disease develop a rash or hard nodules on the soles of their feet or palms of their hands.

The National Institute of Arthritis and Musculoskeletal and Skin Diseases answers your questions about reactive arthritis. 

 

Lupus

Lupus is a chronic autoimmune disease, meaning the body's immune system creates antibodies that attack healthy tissues, including the joints. The wrist and small joints of the hands are among those most commonly affected by lupus. Lupus can also cause inflammation in many organs, including the skin, heart, lungs and kidneys.

Read the latest news headlines about lupus.

 

Psoriatic arthritis

Psoriatic arthritis is a form of arthritis accompanied by the skin disease psoriasis. The skin disease often precedes the arthritis; in a small percentage the joint disease develops before the skin disease. The joint involvement of psoriatic arthritis often causes inflammation of the entire finger, giving it a sausage-like appearance. Approximately 80 percent of people with psoriatic arthritis experience changes to the nails including pitting, thickening and/or separation from the nail bed. The skin rash of psoriatic arthritis can also affect the hands.

Learn more about psoriatic arthritis.

Infectious arthritis

Also called septic arthritis, infectious arthritis refers to arthritis that is caused by an infection within the joint. Infectious arthritis is often caused by bacteria that spread through the bloodstream to the joint. Sometimes it is caused by viruses or fungi and can affect the joints of the hands.

septic arthritis from the National Library of Medicine

 

Raynaud's phenomenon

Raynaud’s phenomenon is a condition characterized by a narrowing of the blood vessels to the extremities, usually the hands, in response to cold temperatures or stress. When blood vessels close down, fingers become cold and white, then blue, and numb or painful. When the vessels open up again, the hands become red or purple. Raynaud’s is often associated with connective tissue diseases, notably scleroderma.

The connection between Raynaud's and alcohol and smoking.

 

 Osteoporosis

 Osteoporosis is a condition in which the bones lose enough mass that they become brittle and prone to breaking with slight trauma. The bones of the wrist are among those most commonly fractured in people with osteoporosis. The condition can occur with aging, inflammatory disease (such as rheumatoid arthritis) inactivity, a low-calcium diet or use of corticosteroid medications.

Find out if you are at risk for osteoporosis.

Find answers to your questions about osteoporosis.

 

Carpal Tunnel syndrome

This condition occurs when the median nerve, a nerve that runs from the forearm into the hand and supplies sensation to the palm and thumb side of the hand, becomes compressed within the carpal tunnel in the wrist. The carpal tunnel is a narrow passageway formed by bones and a ligament, through which the median nerve and several tendons run. If there is swelling within the tunnel, the nerve can become compressed, resulting in pain, weakness, and/or numbness in the hand and wrist, radiating up the arm.

Carpal tunnel syndrome from Arthritis Today.

Carpal tunnel syndrome from the National Institute of Neurological Disorders and Stroke.

Learn about risk factors for carpal tunnel syndrome.

 

Scleroderma

Literally translated "hard skin," scleroderma is an umbrella term for disorders that involve the abnormal growth of the connective tissue supporting the skin and internal organs. Although there are several different forms of scleroderma, all can cause thickening and tightening of the skin on the fingers called sclerodactyly. This can make it harder to bend or straighten the fingers.

Learn more about scleroderma.

 

Dermatomyositis

Dermatomyositis is an inflammatory muscle disease that often has a severe onset. Symptoms can include muscle pain and weakness, joint pain, skin rash, changes around the beds of the fingernails and roughening and cracking of the skin on the palms and fingertips, often referred to as Mechanic's hands.

 The National Institute of Neurological Disorders and Stroke

 

Dupuytren’s contracture

  Dupuytren's contracture, sometimes called Dupuytren's disease, is an abnormal thickening of the fascia, a flat band of tissue beneath the skin, in the palm of the hand. This can lead to the development of firm cords and lumps that cause the fingers to bend toward the palm. The ring and little finger are most commonly affected.  The disease, which occurs primarily in men older than age 40 of European descent, less commonly affects the fascia on the soles of the feet.

 Dupuytren's contracture from the American Academy of Orthopaedic Surgeons. 

 

Ganglion cysts

  Ganglion cysts are lumps that form next to the joints or tendons in the hand and wrist. The most common locations are the joints at the base of the fingers (metacarpophalangeal joint or MCP), joints closest to the nail (distal phalangeal joint or DP), the top of the wrist and the palm side of the wrist. These cysts can occur in people of any age, they may come and go for no apparent reason, and they may or may not be painful.

 The American Academy of Orthopaedic Surgeons.

 

Stenosing tenosynovitis (trigger finger)

This condition, also known as trigger finger, occurs when the pulley (one of the rings connective tissue that hold tendons of the fingers close to the bone) at the base of a finger or thumb thickens, constricting the tendon that enables the finger to move. This can cause popping, pain or a catching feeling in the finger or thumb. In some cases, repeated use can worsen inflammation and make it difficult to straighten or bend the finger.
trigger finger from the American Academy of Orthopaedic Surgeons

 

Arthritis Today

Related articles

• How Much Prescription Medication Online Can A Person Buy (bigsexymedia.com)
• Arthritis is Australia's most chronic condition (bupa.com.au)
• Phil Mickelson's psoriatic arthritis explained (kevinmd.com)
• Nearly 1 In 4 People With Psoriasis May Have Undiagnosed Psoriatic Arthritis (medicalnewstoday.com)

Does CCSVI Cause Multiple Sclerosis?

Even though Canadian researchers found that a considerably higher percentage of MS patients have CCSVI (chronic cerebrospinal venous insufficiency), they still do not know whether CCSVI causes MS or whether there is just a higher rate of CCSVI among MS patients for another reason. The scientists reported their latest finding in CMAJ (Canadian Medical Association Journal).

CCSVI, also known as CCVI or chronic cerebrospinal venous insufficiency is when blood from in the veins which drain the central nervous system are compromised. The term was coined by Paolo Zamboni in 2008. Blood from the brain and spine has trouble getting back to the heart - CCSVI is a chronic (long-term) problem.

The problem is caused by stenosis, narrowing of the veins that drain the spine and brain - resulting in a much longer period for that blood to return to the heart. The blood can reflux back into the spine and brain, edema can occur, and red blood cells and fluids can leak into other tissues of the brain and spine. The blood stays in the brain too long, leading to slowed perfusion (a delay in deoxygenated blood leaving the head), causing hypoxia in the brain. Hypoxia means lack of oxygen. Plasma and iron and other undesirable cells can cross the blood-brain barrier, causing damage.

Zamboni hypothesized at the time that CCSVI played a role in causing MS (multiple sclerosis).

Some studies have not been able to replicate Zamboni's findings - that CCSVI is more prevalent among people with MS.

Scientists from St. Michael's Hospital, University of Toronto, and Sunnybrook Health Sciences Centre, Toronto, and the University of Calgary, Alberta, carried out a meta-analysis - they examined 8 studies that had been carried out in Jordan, Germany, Italy and the USA - and compared CCSVI frequency in patients with MS and without MS.

Some of the studies were incomplete while others were small, as were descriptions of the training of those carrying out the ultrasound studies. None of the studies reported whether those performing the ultrasound scans were working blind or not (whether they knew whether each patient had or did not have MS).

CCSVI rates varied enormously among multiple sclerosis patients across the different studies, from zero per cent to 100% in the one Zamboni carried out. Some studies found higher CCSVI rates among those in the MS groups, while others found no difference.

When they gathered the data from all the studies and combined them, they did find a significantly higher rate of CCSVI among those with MS.
 

Dr. Andreas Laupacis, Li Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, wrote:

"We found a strong and statistically significant association between chronic cerebrospinal venous insufficiency and multiple sclerosis. However, the large amount of heterogeneity among the study results prevents a definitive conclusion. The source of the heterogeneity is not clear. It is not obviously caused by differences in the definition of chronic cerebrospinal venous insufficiency, patient characteristics or the methodologic quality of the studies.

We also could not identify any factor that accounted for the large and problematic difference between the studies in the frequency of chronic cerebrospinal venous insufficiency among patients with multiple sclerosis."

The authors believe the discrepancies in CCSVI rates were mainly due to the size of some of the studies, they were very small - also, there were some serious differences in techniques used for ultrasound as well as quality control. For studies involving ultrasonography, the training and competence of the operators is crucial.

The authors cautioned:

"(a link between CCSVI and MS) does not mean that the condition causes multiple sclerosis."

All we know now is that CCSVI is more common among MS patients - this could be simply because of that, there is a higher risk of CCSVI with MS, or that CCSVI raises the risk of developing MS - nobody currently knows for certain which one it is.

The investigators wrote in conclusion:

"Further high-quality studies, using identical ultrasound protocols, are needed to definitively determine whether chronic cerebrospinal venous insufficiency is more frequent among patients with multiple sclerosis than among those without it."

Dr. Robert Fox wrote in a related Commentary in the same journal:

"The meta-analysis by Laupacis and colleagues is a good starting point; however, much work remains to be done before we can be certain whether chronic cerebrospinal venous insufficiency is a paradigm shift in the classic sense. . . . or just another fad."

Further information on CCSVI-

CCSVI stands for “Chronic Cerebrospinal Venous Insufficiency,” a condition where people have obstructed blood flow in the veins that drain the central nervous system (the brain and spinal cord). Research indicates that CCSVI is significantly correlated with multiple sclerosis.^{1, 2,3,4}

As a result of these venous abnormalities, the blood flow rate through the central nervous system back toward the heart may become slowed, and blood may reflux back toward the brain and spine.¹

People with CCSVI have one or more of the following blockages of the veins that drain blood from the central nervous system:

• Stenosis is an abnormal narrowing of the veins that restricts blood flow. Types of stenoses include the collapse of the vein, twisting of the vein, ring-like narrowings in the vein, and other similar obstructions
• An abnormal valve, septum, flap, or membrane that blocks or inhibits blood flow through the veins
• Atresia, hypoplasia, or agenesis are severe venous problems, including veins that are partially closed, underdeveloped, minimally formed, or almost entirely missing

The animation below shows how stenosis in veins draining the central nervous system can cause CCSVI. This animation was provided by Dr. Zamboni.

Medical News Today

CCSVI Alliance

 

Related articles

 

• Some link between CCSVI and MS but quality of evidence prevents definitive conclusion (eurekalert.org)
• A CCSVI Meta-Analysis (theness.com)
• Over $2.4 Million Committed to Support 7 Initial CCSVI Grants to Determine the Role of CCSVI (Venous Insufficiency) in Multiple Sclerosis Disease Process (prweb.com)
• Liberation therapy: the 'wave of complications' breaks (macleans.ca)
• Zivadinov's Update On Chronic Cerebrospinal Venous Insufficiency (CCSVI) In Multiple Sclerosis (prweb.com)